Impact of native-plants policy scenarios on premature mortality in Denver: A quantitative health impact assessment.

BACKGROUND: Cities often use non-native plants such as turf grass to expand green space. Native plants, however, may require less water and maintenance and have co-benefits for local biodiversity, including pollinators. Previous studies estimating mortality averted by adding green space have not considered the provision of native plants as part of the greening policies. AIM: We aim to estimate premature deaths that would be prevented by the implementation of native-plants policy scenarios in the City of Denver, Colorado, USA. METHODS: After conducting interviews with local expert stakeholders, we designed four native-plants policy scenarios: (1) greening 30% of all city census-block groups to the greenness level of native plants, (2) adding 200-foot native-plants buffers around riparian areas, (3) constructing large water retention ponds landscaped with native plants, and (4) greening parking lots. We defined the normalized difference vegetation index (NDVI) corresponding to native plants by measuring the NDVI at locations with known native or highly diverse vegetation. Using a quantitative health-impact assessment approach, we estimated premature mortality averted under each scenario, comparing alternative NDVI with the baseline value. RESULTS: In the most ambitious scenario, we estimated that 88 (95% uncertainty interval (UI): 20, 128) annual premature deaths would be prevented by greening 30% of the area of census block groups with native plants. We estimated that greening 30% of parking-lot surface with native plants would prevent 14 annual deaths (95% UI: 7, 18), adding the native buffers around riparian areas would prevent 13 annual deaths (95% UI: 2, 20), and adding the proposed stormwater retention ponds would prevent no annual deaths (95% UI: 0, 1). CONCLUSION: Using native plants to increase green spaces has the potential to prevent premature deaths in the City of Denver, but results were sensitive to the definition of native plants and the policy scenario.

Contribution of N-methyl-D-aspartate receptors to attention and episodic spatial memory during senescence.

A decrease in N-methyl-D-aspartate receptor (NMDAR) function is associated with age-related cognitive impairments. However, NMDAR antagonists are prescribed for cognitive decline associated with age-related neurodegenerative disease, raising questions as to the role of NMDAR activity in cognitive function during aging. The current studies examined effects of NMDAR blockade on cognitive task that are sensitive to aging. Young and middle-age rats were trained on the five-choice serial reaction time task (5-CSRTT) and challenged with MK-801 (0.025, 0.05, and 0.1mg/kg or vehicle). Attention deficits were apparent in middle-age and performance of young and middle-age rats was enhanced for low doses of MK-801 (0.025 and 0.05). The beneficial effects on attention were reversed by the highest dose of MK-801. Older animals exhibited a delay-dependent impairment of episodic spatial memory examined on a delayed-matching to place water maze task. Similarly, a low dose of MK-801 (0.05mg/kg) impaired performance with increasing delay and aged animals were more susceptible to disruption by NMDAR blockade. Despite MK-801 impairment of episodic spatial memory, MK-801 had minimal effects on spatial reference memory. Our results confirm that NMDARs contribute to rapidly acquired and flexible spatial memory and support the idea that a decline in NMDAR function contributes to the age-related impairments in cognition.

Impaired attention and synaptic senescence of the prefrontal cortex involves redox regulation of NMDA receptors.

Young (3-6 months) and middle-age (10-14 months) rats were trained on the five-choice serial reaction time task. Attention and executive function deficits were apparent in middle-age animals observed as a decrease in choice accuracy, increase in omissions, and increased response latency. The behavioral differences were not due to alterations in sensorimotor function or a diminished motivational state. Electrophysiological characterization of synaptic transmission in slices from the mPFC indicated an age-related decrease in glutamatergic transmission. In particular, a robust decrease in N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic responses in the mPFC was correlated with several measures of attention. The decrease in NMDAR function was due in part to an altered redox state as bath application of the reducing agent, dithiothreitol, increased the NMDAR component of the synaptic response to a greater extent in middle-age animals. Together with previous work indicating that redox state mediates senescent physiology in the hippocampus, the results indicate that redox changes contribute to senescent synaptic function in vulnerable brain regions involved in age-related cognitive decline.

Assessing the emergence and reliability of cognitive decline over the life span in Fisher 344 rats using the spatial water maze.

The spatial water maze is routinely used to investigate hippocampal-dependent spatial memory and the biological mechanisms that underlie variability in cognitive decline during aging. The utility of the task for repeated testing in order to examine the trajectory of cognitive decline and to prescreen animals prior to therapeutic interventions maybe limited due to carryover effects of repeated training. The current study examines the role of carryover effects, as well as the reliability of individual differences, in determining age-related impairment on episodic and reference memory versions of the water maze task. Results indicate that impaired acquisition of episodic spatial information emerges in middle-age and the propensity for impairment increases with advancing age. While learning was variable across animals, acquisition deficits for episodic information were reliable across training sessions in middle-age and aged rats. A significant impairment in the 24~h retention of episodic spatial information was observed in aged animals. When animals were trained to the same location (i.e., reference memory), an impairment was limited to the rate of acquisition in aged animals. However, with continued training, all aged animals were able to acquire a reference memory and no age differences were observed in the 24~h retention of a spatial reference memory. Together, the results point to a progressive impairment in episodic spatial memory with advancing age and suggest that tests of episodic spatial memory are reliable and more sensitive than reference memory for detecting cognitive decline.

Behavioral model for assessing cognitive decline.

The water maze task can be used to assess sensory motor and cognitive function in rodents. When properly employed, this task can behaviorally assess acquisition of a spatial search strategy, as well as working and reference memory. The following section uses research on age-related, cognitive decline to illustrate the methods employed and highlight areas that can, if not properly controlled, confound a study.

In vivo pharmacological manipulation of small conductance Ca(2+)-activated K(+) channels influences motor behavior, object memory and fear conditioning.

Small conductance Ca(2+)-activated K(+) channels (SK, K(Ca2.1), K(Ca2.2), K(Ca2.3)) are expressed at high levels in brain regions critical for learning and memory. The activation of dendritic SK channels limits the induction of synaptic plasticity that may underlie hippocampal and amygdala dependent memory. EBIO facilitates SK channel activation by increasing their sensitivity to calcium. The compound CyPPA selectively activates SK2 and SK3 channels in a similar manner. To date there has been no report of the effects of SK channel activators on memory. Therefore, the present study examined the effects of systemic EBIO on mice in a behavioral task battery. Significant effects of EBIO on memory and motor activity were validated and extended by examining the effects of systemic CyPPA. Systemic EBIO and CyPPA both produced a transient decline in locomotor behavior. Neither SK channel activator affected anxiety. EBIO (17.5 mg/kg) impaired the encoding, but not retrieval, of object memory in a spontaneous object recognition task. A similar impairment of object memory encoding was observed in CyPPA (15 mg/kg)-treated mice. These memory-impairing effects were not due to changes in motivation, attention or movement. Systemic EBIO did not affect contextual or cued fear memory after conditioning with a 3 tone (CS)-footshock (US) pairing protocol or a 1 CS-US pairing protocol. Interestingly, apamin (0.4 mg/kg) enhanced contextual fear memory in mice conditioned with a 1 CS-US pairing protocol. These results suggest that SK channel activation impairs the encoding of non-aversive memory but not memory for aversive events. These data support converging evidence that SK channels regulate cellular mechanisms of memory encoding.